Expression profile of integrin family genes in patients with myocardial infarction and in healthy subjects: an oligonucleotide microarray and QRT-PCR assessment. Preliminary results

Pathogenesis and clinical course of all known cardiovascular diseases are rooted in endothelial dysfunction. Coronary thrombosis which can aggravate the coronary condition leading to myocardial infarction (MI) is closely linked to cellular adhesion processes involving numerous adhesion molecules. Th...

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Bibliographic Details
Published inMinerva medica Vol. 110; no. 3; p. 224
Main Authors Głogowska-Ligus, Joanna, Dąbek, Józefa
Format Journal Article
LanguageEnglish
Published Italy 01.06.2019
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Summary:Pathogenesis and clinical course of all known cardiovascular diseases are rooted in endothelial dysfunction. Coronary thrombosis which can aggravate the coronary condition leading to myocardial infarction (MI) is closely linked to cellular adhesion processes involving numerous adhesion molecules. The goal of our study was to find and quantitate the expression of integrin genes that differentiate between MI patients and healthy subjects. The study included 171 individuals, among whom 8 were chosen to provide study material for the oligonucleotide microarray investigation (4 MI patients and 4 healthy subjects). The investigated material consisted of RNA isolated from peripheral blood mononuclear cells. Analysis of gene expression data from eight HG-U133A microarrays allowed identification of three genes differentiating the examined groups. The differentiating genes were found using the Bland-Altman method. Two of them showed increased expression (beta 2 integrin and beta 7 integrin genes), whereas expression level of the third (beta 3 integrin gene) was decreased. The differences in integrin gene expression levels that were observed in MI patients, as compared to healthy individuals, might be responsible for endothelial dysfunction as well as rise in adhesion and aggregation processes in this group of patients and might lead to coronary vessel occlusion by thrombi and myocardial infarction.
ISSN:1827-1669
DOI:10.23736/S0026-4806.19.05842-7